Impact of Post-Exercise Muscle Oxygen Saturation Levels on Measurements of Metabolic Rate Measured with Near Infrared Spectroscopy

Abstract

Skeletal muscle oxidative capacity has been characterized by measuring post-exercise recovery kinetics of muscle oxygen consumption using near infrared spectroscopy (NIRS). Preliminary observations have suggested that low post-exercise muscle oxygen saturation (O2sat) may influence measurements of oxidative capacity. PURPOSE: To determine if post-exercise O2sat levels influenced metabolic rates as measured by NIRS. METHODS: Healthy male subjects were tested (n = 7, age = 27 ± 3 years). Post-exercise measurements of O2sat, metabolic rate, and oxidative capacity were performed on the wrist-flexor muscles using NIRS. O2sat levels were reduced using two durations (10 and 20s) of voluntary wrist flexor exercise. To control for the influence of exercise duration, electrical stimulation (e-stim) (frequency: 5 Hz, duration: 10 and 20s) was used to induce muscle activation without significantly reducing O2sat. RESULTS: O2sat following 20s of voluntary exercise was ∼45% lower than after 10s (10s: 73.4 ± 3.6 %; 20 s: 46.3 ± 8.6 %). In contrast, O2sat following 20s of e-stim was only ∼9% lower than after 10s (10s: 85.9 ± 3.6 %; 20s: 78.5 ± 6.8 %, p < 0.05). Increased duration of voluntary exercise did not result in increased post-exercise metabolic rate (10s: 4.7 ± 0.95 %/s, 20s: 5.0 ± 1.1 %/s, p > 0.05). However, electrical stimulation post-exercise metabolic rates were increased ∼50% with increasing duration of e-stim (10s: 3.0 ± 0.9 %/s, 20s: 5.0 ± 1.0 %/s, p < 0.05). Importantly, oxidative capacity following 20s of voluntary exercise was significantly lower than all other conditions (0.87 ± 0.16 min-1, p < 0.05), and no difference was found between the 10 and 20 s e-stim and the 10 s voluntary conditions (e-stim 10: 1.7 ± 0.3, e-stim 20: 1.7 ± 0.2, voluntary 10: 1.6 ± 0.2 min-1, p > 0.05). CONCLUSION: These results suggest that exercise, which significantly lowers O2sat blunts metabolic rate, resulting in artificially slow measurements of oxidative capacity measured by NIRS. A potential explanation for this is that low oxygen levels may limit oxygen transport to skeletal muscle mitochondria.